Antiviral reactivities of γδ T cells (original) (raw)

γδ T lymphocyte responses to HIV

Clinical & …, 1996

Natural immunity may be involved in controlling viral spread in hosts infected with HIV. A panel of T cell receptor-positive lymphocyte clones was isolated from the peripheral blood of healthy HIV ÿ donors and tested for anti-HIV cytotoxic responses. Twelve of 30 (40%) V 9 = V2 T cell clones, but none of seven V1 T cell clones, displayed lytic activity against HIV-infected cells. The V 9 = V2 clones cytotoxic for HIV-infected cells also lysed Daudi cells. However, not all V 9 /V2 clones which lysed Daudi targets had the capacity to lyse HIV-infected cells. Some of the T cell clones were also investigated for potential proliferative responses to HIV-infected cells. One V 9 = V2 T cell clone (ME8-7) and one V1 T cell clone (ME18-2) demonstrated proliferative responses toward HIVinfected cells. Another V 9 = V2 clone (VM39) proliferated in response to cell-free HIV. Taken together, these results provide direct evidence of anti-HIV T cell responses in healthy, HIV ÿ persons.

Innate Immunity to Viruses: Control of Vaccinia Virus Infection by γδ T Cells

The Journal of Immunology, 2001

The existence of γδ T cells has been known for over 15 years, but their significance in innate immunity to virus infections has not been determined. We show here that γδ T cells are well suited to provide a rapid response to virus infection and demonstrate their role in innate resistance to vaccinia virus (VV) infection in both normal C57BL/6 and β TCR knockout (KO) mice. VV-infected mice deficient in γδ T cells had significantly higher VV titers early postinfection (PI) and increased mortality when compared with control mice. There was a rapid and profound VV-induced increase in IFN-γ-producing γδ T cells in the peritoneal cavity and spleen of VV-infected mice beginning as early as day 2 PI. This rapid response occurred in the absence of priming, as there was constitutively a significant frequency of VV-specific γδ T cells in the spleen in uninfected β TCR KO mice, as demonstrated by limiting dilution assay. Also, like NK cells, another mediator of innate immunity to viruses, γδ T ...

Mechanisms of induction of primary virus-specific cytotoxic T lymphocyte responses

European Journal of Immunology, 1992

Mechanisms of induction of primary virus-specific cytotoxic T lymphocyte responses* We have investigated the ability of various antigen-presenting cell (APC) types to induce primary anti-viral cytotoxic T lymphocyte (CTL) responses by single in vitro stimulation. Of these APC types, only dendritic cells (DC) and RMA-S lymphoma cells could induce primary CTL responses, but by divergent mechanisms. DC were capable of generating primary virus-specific CTL, either by presenting viral peptide or processed infectious virus. In contrast, RMA-S cells could not present endogenous antigen, e.g. after virus infection, but this cell line very efficiently presented exogenous viral peptides to induce primary virusspecific CTL in vitro. Spleen cells, lipopolysaccharide-induced B cell blasts or the non-mutated RMA cells did not have the ability to trigger unprimed T cells by single in vitro stimulation. We have investigated several characteristics important for primary CTL response induction by DC and RMA-S cells (summarized in Fig. 6). Primary CTL response induction by DC or RMA-S cells was blocked by anti-LFA-1 or anti-CD8 monoclonal antibodies (mAb). DC rapidly aggregated with unprimed T cells, which was independent of LFA-1 and CD8 molecules. RMA-S cells did not form conjugates with unprimed Tcells. Despite their abundant major histocompatibility complex (MHC) class I cell-surface expression, DC did not bind much exogenously added viral peptide. In contrast, the MHC class I molecules on RMA-S cells bound a large quantity of exogenously administered peptide. Powerful adhesion by DC and high expression of relevant MHC/peptide complexes on RMA-S cells are important features in the initial contact with unprimed T lymphocytes. In a later stage of contact, both DC and RMA-S cells activate LFA-1 (and CD8) molecules at the Tcell surface to strengthen and maintain the contact between T cell and APC. * This work was supported by the Netherlands Organization for Scientific Research (NWO) grants 900-500-092 and 900-507-122. Fellow of the Royal Netherlands Academy of Arts and Sciences (KNAW) .

Human γδ T-cell responses in infection and immunotherapy: Common mechanisms, common mediators?

European Journal of Immunology, 2012

[Tonegawa, S., Scand. J. Immunol. 1993. 38: 303-319]. Twenty-five years of intense research later this ambivalent view still holds true. Immunologists now appreciate that γδ T cells indeed represent a highly intriguing "new aspect of immunity" that is unique and distinct from conventional lymphocytes, yet even scientists in the field still struggle to understand the molecular basis of γδ T-cell responses, especially with respect to the enigmatic mode of antigen recognition. Here, we portray the peculiar responsiveness of human Vγ9/Vδ2 T cells to microorganisms, tumor cells and aminobisphosphonates, in an attempt to integrate the corresponding -and at times confusing -findings into a "theory of everything" that may help explain how such diverse stimuli result in similar γδ T-cell responses via the recognition of soluble low molecular weight phosphoantigens.

Vaccinia Virus Inhibits T Cell Receptor–Dependent Responses by Human γδ T Cells

The Journal of Infectious Diseases, 2007

Vaccinia virus (VV), a member of the poxvirus family, has been used successfully as a vaccine to eradicate human smallpox [1]. With DNA replication occurring exclusively in the cytosol and the ability to induce both cellular and humoral immunity, VV has also been championed as a live recombinant vaccine vector that promotes immunity against tumors and infectious diseases . Although VV can induce strong humoral and cellular immune responses to viral and recombinant antigens, it is also known that poxviruses employ many mechanisms to evade host immunity. VV gene products block complement, cytokines, and chemokines; they also prevent apoptosis and interfere with intracellular signaling . VV modulates the function of NK cells , inhibits the maturation of human dendritic cells , and disrupts major histocompatibility complex (MHC) class I or II-mediated antigen presentation . The effects that VV has on another important cell type, gd T cells, is poorly understood.

T lymphocyte response to flavivirus infections

1989

X interaction with uninfected targets as determined by blocking of lysis with anti-CDS monoclonal antitxxiy supporting the existence of a low avidity and high avidity self-reactive Tc cells. It is postulated that these findings have important implications for virus-induced autoimmune phenomena. CHAPTER 1. GENERAL INTRODUCTION.